CoChat
Sign Up
Cited by 716

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Genomic instability and myelodysplasia with monosomy 7 consequent to EVI1 activation after gene therapy for chronic granulomatous disease

Stein, Stefan, Ott, Marion G, Schultze-Strasser, Stephan, Jauch, Anna, Burwinkel, Barbara, Kinner, Andrea, Schmidt, Manfred, Krämer, Alwin, Schwäble, Joachim, Glimm, Hanno, Koehl, Ulrike, Preiss, Carolin, Ball, Claudia, Martin, Hans, Göhring, Gudrun, Schwarzwaelder, Kerstin, Hofmann, Wolf-Karsten, Karakaya, Kadin, Tchatchou, Sandrine, Yang, Rongxi, Reinecke, Petra, Kühlcke, Klaus, Schlegelberger, Brigitte, Thrasher, Adrian J, Hoelzer, Dieter, Seger, Reinhard, von Kalle, Christof, Grez, Manuel·2010·Nature Medicine
DOI 10.1038/nm.2088
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1038/nm.2088

Cites

5 of 5 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 54

  1. Cavazzana-Calvo, M. et al. Gene therapy of human severe combined immunodeficiency (SCID)-X1 disease. Science 288, 669–672 (2000). · DOI · Paper page
  2. Aiuti, A. et al. Correction of ADA-SCID by stem cell gene therapy combined with nonmyeloablative conditioning. Science 296, 2410–2413 (2002). · DOI · Paper page
  3. Gaspar, H.B. et al. Gene therapy of X-linked severe combined immunodeficiency by use of a pseudotyped gammaretroviral vector. Lancet 364, 2181–2187 (2004). · DOI
  4. Gaspar, H.B. et al. Successful reconstitution of immunity in ADA-SCID by stem cell gene therapy following cessation of PEG-ADA and use of mild preconditioning. Mol. Ther. 14, 505–513 (2006). · DOI
  5. Aiuti, A. et al. Gene therapy for immunodeficiency due to adenosine deaminase deficiency. N. Engl. J. Med. 360, 447–458 (2009). · DOI
  6. Hacein-Bey-Abina, S. et al. LMO2-associated clonal T cell proliferation in two patients after gene therapy for SCID-X1. Science 302, 415–419 (2003). · DOI · Paper page
  7. Howe, S.J. et al. Insertional mutagenesis combined with acquired somatic mutations causes leukemogenesis following gene therapy of SCID-X1 patients. J. Clin. Invest. 118, 3143–3150 (2008). · DOI · Paper page
  8. Dinauer, M.C. The respiratory burst oxidase and the molecular genetics of chronic granulomatous disease. Crit. Rev. Clin. Lab. Sci. 30, 329–369 (1993). · DOI
  9. Roos, D. The genetic basis of chronic granulomatous disease. Immunol. Rev. 138, 121–157 (1994). · DOI
  10. Segal, A.W. The NADPH oxidase and chronic granulomatous disease. Mol. Med. Today 2, 129–135 (1996). · DOI
  11. Malech, H.L. & Hickstein, D.D. Genetics, biology and clinical management of myeloid cell primary immune deficiencies: chronic granulomatous disease and leukocyte adhesion deficiency. Curr. Opin. Hematol. 14, 29–36 (2007). · DOI · Paper page
  12. Ott, M.G. et al. Correction of X-linked chronic granulomatous disease by gene therapy, augmented by insertional activation of MDS1–EVI1, PRDM16 or SETBP1. Nat. Med. 12, 401–409 (2006). · DOI · Paper page
  13. Fears, S. et al. Intergenic splicing of MDS1 and EVI1 occurs in normal tissues as well as in myeloid leukemia and produces a new member of the PR domain family. Proc. Natl. Acad. Sci. USA 93, 1642–1647 (1996). · DOI
  14. Hamaguchi, H. et al. Establishment of a novel human myeloid leukaemia cell line (HNT-34) with t(3;3)(q21;q26), t(9;22)(q34;q11) and the expression of EVI1 gene, P210 and P190 BCR/ABL chimaeric transcripts from a patient with AML after MDS with 3q21q26 syndrome. Br. J. Haematol. 98, 399–407 (1997). · DOI
  15. Claus, R. & Lubbert, M. Epigenetic targets in hematopoietic malignancies. Oncogene 22, 6489–6496 (2003). · DOI
  16. Nolte, F. & Hofmann, W.K. Myelodysplastic syndromes: molecular pathogenesis and genomic changes. Ann. Hematol. 87, 777–795 (2008). · DOI
  17. Christiansen, D.H., Andersen, M.K. & Pedersen-Bjergaard, J. Methylation of p15INK4B is common, is associated with deletion of genes on chromosome arm 7q and predicts a poor prognosis in therapy-related myelodysplasia and acute myeloid leukemia. Leukemia 17, 1813–1819 (2003). · DOI
  18. Khanna, K.K. & Jackson, S.P. DNA double-strand breaks: signaling, repair and the cancer connection. Nat. Genet. 27, 247–254 (2001). · DOI · Paper page
  19. Fernandez-Capetillo, O., Celeste, A. & Nussenzweig, A. Focusing on foci: H2AX and the recruitment of DNA-damage response factors. Cell Cycle 2, 426–427 (2003). · DOI
  20. Kearns, W.G., Yamaguchi, H., Young, N.S. & Liu, J.M. Centrosome amplification and aneuploidy in bone marrow failure patients. Genes Chromosomes Cancer 40, 329–333 (2004). · DOI
  21. Neben, K., Giesecke, C., Schweizer, S., Ho, A.D. & Kramer, A. Centrosome aberrations in acute myeloid leukemia are correlated with cytogenetic risk profile. Blood 101, 289–291 (2003). · DOI
  22. Ganem, N.J., Godinho, S.A. & Pellman, D. A mechanism linking extra centrosomes to chromosomal instability. Nature 460, 278–282 (2009). · DOI
  23. Dinauer, M.C., Curnutte, J.T., Rosen, H. & Orkin, S.H. A missense mutation in the neutrophil cytochrome b heavy chain in cytochrome-positive X-linked chronic granulomatous disease. J. Clin. Invest. 84, 2012–2016 (1989). · DOI
  24. Wang, L., Robbins, P.B., Carbonaro, D.A. & Kohn, D.B. High-resolution analysis of cytosine methylation in the 5′ long terminal repeat of retroviral vectors. Hum. Gene Ther. 9, 2321–2330 (1998). · DOI
  25. Frank, O. et al. Tumor cells escape suicide gene therapy by genetic and epigenetic instability. Blood 104, 3543–3549 (2004). · DOI
  26. Burns, W.R., Zheng, Z., Rosenberg, S.A. & Morgan, R.A. Lack of specific gamma-retroviral vector long terminal repeat promoter silencing in patients receiving genetically engineered lymphocytes and activation upon lymphocyte restimulation. Blood 114, 2888–2899 (2009). · DOI
  27. Metais, J.Y. & Dunbar, C.E. The MDS1–EVI1 gene complex as a retrovirus integration site: impact on behavior of hematopoietic cells and implications for gene therapy. Mol. Ther. 16, 439–449 (2008). · DOI
  28. Du, Y., Jenkins, N.A. & Copeland, N.G. Insertional mutagenesis identifies genes that promote the immortalization of primary bone marrow progenitor cells. Blood 106, 3932–3939 (2005). · DOI
  29. Calmels, B. et al. Recurrent retroviral vector integration at the MDS1–EVI1 locus in non-human primate hematopoietic cells. Blood 106, 2530–2533 (2005). · DOI
  30. Li, Z. et al. Murine leukemia induced by retroviral gene marking. Science 296, 497 (2002). · DOI · Paper page
  31. Modlich, U. et al. Leukemia induction after a single retroviral vector insertion in Evi1 or Prdm16. Leukemia 22, 1519–1528 (2008). · DOI
  32. Buonamici, S. et al. EVI1 induces myelodysplastic syndrome in mice. J. Clin. Invest. 114, 713–719 (2004). · DOI
  33. Du, Y., Spence, S.E., Jenkins, N.A. & Copeland, N.G. Cooperating cancer-gene identification through oncogenic-retrovirus-induced insertional mutagenesis. Blood 106, 2498–2505 (2005). · DOI
  34. Nucifora, G. The EVI1 gene in myeloid leukemia. Leukemia 11, 2022–2031 (1997). · DOI
  35. Dreyfus, F. et al. Expression of the Evi-1 gene in myelodysplastic syndromes. Leukemia 9, 203–205 (1995).
  36. Barjesteh van Waalwijk van Doorn-Khosrovani, S et al. High EVI1 expression predicts poor survival in acute myeloid leukemia: a study of 319 de novo AML patients. Blood 101, 837–845 (2003). · DOI
  37. Charrin, C. et al. Structural rearrangements of chromosome 3 in 57 patients with acute myeloid leukemia: clinical, hematological and cytogenetic features. Hematol. J. 3, 21–31 (2002). · DOI
  38. Lin, P., Medeiros, L.J., Yin, C.C. & Abruzzo, L.V. Translocation (3;8)(q26;q24): a recurrent chromosomal abnormality in myelodysplastic syndrome and acute myeloid leukemia. Cancer Genet. Cytogenet. 166, 82–85 (2006). · DOI
  39. Stevens-Kroef, M. et al. Translocation t(2;3)(p15–23;q26–27) in myeloid malignancies: report of 21 new cases, clinical, cytogenetic and molecular genetic features. Leukemia 18, 1108–1114 (2004). · DOI
  40. Trubia, M. et al. Characterization of a recurrent translocation t(2;3)(p15–22;q26) occurring in acute myeloid leukaemia. Leukemia 20, 48–54 (2006). · DOI
  41. Laricchia-Robbio, L. & Nucifora, G. Significant increase of self-renewal in hematopoietic cells after forced expression of EVI1. Blood Cells Mol. Dis. 40, 141–147 (2007). · DOI
  42. Perkins, A.S., Mercer, J.A., Jenkins, N.A. & Copeland, N.G. Patterns of Evi-1 expression in embryonic and adult tissues suggest that Evi-1 plays an important regulatory role in mouse development. Development 111, 479–487 (1991). · DOI
  43. Kustikova, O.S. et al. Retroviral vector insertion sites associated with dominant hematopoietic clones mark “stemness” pathways. Blood 109, 1897–1907 (2007). · DOI
  44. Senyuk, V. et al. Repression of RUNX1 activity by EVI1: a new role of EVI1 in leukemogenesis. Cancer Res. 67, 5658–5666 (2007). · DOI
  45. Chi, Y., Senyuk, V., Chakraborty, S. & Nucifora, G. EVI1 promotes cell proliferation by interacting with BRG1 and blocking the repression of BRG1 on E2F1 activity. J. Biol. Chem. 278, 49806–49811 (2003). · DOI
  46. Cattaneo, F. & Nucifora, G. EVI1 recruits the histone methyltransferase SUV39H1 for transcription repression. J. Cell. Biochem. 105, 344–352 (2008). · DOI
  47. Spensberger, D. & Delwel, R. A novel interaction between the proto-oncogene Evi1 and histone methyltransferases, SUV39H1 and G9a. FEBS Lett. 582, 2761–2767 (2008). · DOI
  48. Spensberger, D. et al. Myeloid transforming protein Evi1 interacts with methyl-CpG binding domain protein 3 and inhibits in vitro histone deacetylation by Mbd3/Mi-2/NuRD. Biochemistry 47, 6418–6426 (2008). · DOI
  49. Kondo, Y. et al. Downregulation of histone H3 lysine 9 methyltransferase G9a induces centrosome disruption and chromosome instability in cancer cells. PLoS One 3, e2037 (2008). · DOI
  50. Krämer, A., Neben, K. & Ho, A.D. Centrosome replication, genomic instability and cancer. Leukemia 16, 767–775 (2002). · DOI
  51. Zhang, Y. et al. MLL5 contributes to hematopoietic stem cell fitness and homeostasis. Blood 113, 1455–1463 (2009). · DOI
  52. Heuser, M. et al. Loss of MLL5 results in pleiotropic hematopoietic defects, reduced neutrophil immune function, and extreme sensitivity to DNA demethylation. Blood 113, 1432–1443 (2009). · DOI
  53. Madan, V. et al. Impaired function of primitive hematopoietic cells in mice lacking the mixed-lineage-leukemia homolog MLL5. Blood 113, 1444–1454 (2009). · DOI
  54. Sebastian, S. et al. MLL5, a trithorax homolog, indirectly regulates H3K4 methylation, represses cyclin A2 expression, and promotes myogenic differentiation. Proc. Natl. Acad. Sci. USA 106, 4719–4724 (2009). · DOI

Cited by

See all 716

Metadata

Authors
Stein, S., Ott, M. G., Schultze-Strasser, S., Jauch, A., Burwinkel, B., Kinner, A., Schmidt, M., Krämer, A., Schwäble, J., Glimm, H., Koehl, U., Preiss, C., Ball, C., Martin, H., Göhring, G., Schwarzwaelder, K., Hofmann, W.-K., Karakaya, K., Tchatchou, S., Yang, R., Reinecke, P., Kühlcke, K., Schlegelberger, B., Thrasher, A. J., Hoelzer, D., Seger, R., von Kalle, C., & Grez, M.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2010-01-24
Volume
16
Issue
2
Pages
198-204
ISSN
  • 1078-8956
  • 1546-170X
DOI
10.1038/nm.2088
Cited by
716
References
5
Language
en
Licence
www.springer.com/tdm (tdm)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review